Enhancement of de Novo Fatty Acid Biosynthesis in Hepatic Cell Line Huh7 Expressing Hepatitis C Virus Core Protein
-
- Fukasawa Masayoshi
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Tanaka Yasuhito
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Sato Shigeko
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Ono Yujin
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Nitahara-Kasahara Yuko
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Suzuki Tetsuro
- Department of Virology II, National Institute of Infectious Diseases
-
- Miyamura Tatsuo
- Department of Virology II, National Institute of Infectious Diseases
-
- Hanada Kentaro
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases
-
- Nishijima Masahiro
- Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases Department of Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Doshisha Women's College of Liberal Arts
この論文をさがす
抄録
Hepatitis C virus (HCV) core protein plays important roles in the pathogeneses of liver steatosis as well as hepatocellular carcinomas due to HCV infection. In this study, we examined de novo fatty acid biosynthesis in hepatic cell line Huh7 cells expressing HCV core protein. The rate of metabolic labeling of cellular fatty acids with [3H]acetate in core-expressing (Uc39-6) cells was ca. 1.5-fold higher than that in non-expressing (Uc321) cells. The enzyme activities responsible for fatty acid biosynthesis were assayed in vitro. Cytosolic acetyl-CoA carboxylase activity in Uc39-6 cells was ca. 1.6-fold higher than that in Uc321 cells. On the other hand, cytosolic fatty acid synthase activity in Uc39-6 cells was only slightly higher than that in Uc321 cells. Immunoblot analysis of acetyl-CoA carboxylase 1 (ACC1), which is a rate-limiting enzyme for fatty acid biosynthesis, revealed a higher expression level of the protein in Uc39-6 cells than in Uc321 cells. The ACC1 mRNA content in Uc39-6 cells was 1.4-fold higher than that in Uc321 cells. These results strongly suggest that enhancement of fatty acid biosynthesis in core-expressing cells is caused by increased expression of fatty acid biosynthetic enzymes, especially ACC1. Up-regulation of de novo fatty acid biosynthesis by HCV core protein may affect cellular lipid metabolism, resulting in neutral lipid accumulation in HCV-infected cells.
収録刊行物
-
- Biological & Pharmaceutical Bulletin
-
Biological & Pharmaceutical Bulletin 29 (9), 1958-1961, 2006
公益社団法人 日本薬学会
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390001204627451520
-
- NII論文ID
- 110005602369
-
- NII書誌ID
- AA10885497
-
- COI
- 1:CAS:528:DC%2BD28XhtFCgtbzP
-
- ISSN
- 13475215
- 09186158
-
- NDL書誌ID
- 8026924
-
- PubMed
- 16946517
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可